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The Missing Link Between Psychology and Biology
The distinction between mind and body was unfortunately made centuries ago and remains with us today. We label illnesses caused by germs or viruses as “physical”. We label other illnesses such as depression and anxiety as “mental”. Yet the distinction between mental and physical is often unclear. For example, placebos are substances, such as sugar pills, that are thought to be physically inactive but can produce medical benefits in patients who believe they will work.
In my book Cognitive Neuroscience and Psychotherapy: Network Principles for a Unified Theory, I point out that “Kirsch et al. (2008) reported that placebos are about 80% as effective as antidepressant medications are and 50% as effective as analgesic medications are. Kirsch and Sapirstein (1998) estimated that placebos were 75% as effective as antidepressive medications” (p. 252).
The field of psychobiology studies placebo responses and other instances of mind-brain links. The field of biopsychology involves the reverse case; it is concerned with ways that the physical body effects mental states. For example, it studies how legal and illegal psychoactive drugs alter the ways that we think, feel, and act.
Most people probably think of transitional fossils or species when they hear the term “missing link” but another just as important missing link is the one between psychology and biology, between our physical and mental states. The terms psychobiology and biopsychology imply that psychology and biology are connected and interact. The problem with both psychobiology and biopsychology is that there is a missing causal explanatory link between mind and brain.
A very well accepted theoretical orientation in psychological science is the BioPsychoSocial (BPS) model. You might think that this model explains how psychology and biology interact, but you would be wrong. The BPS model is actually just a list of ingredients. It lists important biological, psychological, and social variables and claims that they mutually interact but does not provide any natural science mechanism information that can explain how they interact.
Some authors place these terms in boxes and draw arrows among them to impute causality but never provide any natural science mechanism information that actually explains how they physically interact. In short, the BPS model explains nothing more about how psychology and biology interact than explaining how a car works by listing that it is made of glass, metal, and petroleum. Listing is not explaining. Instead, the missing explanatory link is glossed over in hopes that you will either not notice or ask about it.
The most important task facing psychobiologists and biopsychologists is to provide a natural science explanation that links psychology and biology. This task requires identifying principles that provide mechanism information because mature sciences are organized around principles; psychology is currently not. Those of you who have taken an introductory psychology course or who have read about psychology will recognize that psychology is currently organized around famous people, such as Freud and Skinner, or around “isms” such as behaviorism and cognitivism. This organization differs from all other natural sciences. They are organized around physical entities such as the cell in biology and molecules in chemistry. This allows biologists and chemists to explain more about how things work than psychologists can. Imagine how much better our therapies will become once we understand how and why they work.
I provide some of the missing explanatory details in my book entitled Cognitive Neuroscience and Psychotherapy: Network Principles for a Unified Theory. The remainder of this blog briefly presents the general conceptual framework for understanding how psychology and biology interact that my book is based on. I refer to this explanatory approach as a Bio«Psychology Network (BPN) explanatory system because it consists of four core and now nine corollary principles that together can explain a wide variety of well replicated psychological phenomena in ways that are fully consistent with neuroscience.
The first thing to understand is that our brains are made up of neurons that form neural networks. Hence, some form of network theory is required to explain how psychology and biology interact. How can these neural network models explain psychology? To answer that, we must first recognize that learning and memory form the basis of all psychology. Carlson, Miller, Heth, Donahoe, and Martin (2010) stated that “Learning refers to the process by which experiences change our nervous system and hence our behavior. We refer to these changes as memories” (p. 440; italics in the original). Learning is crucial to human survival. If we could not form memories as infants, we could not learn to do anything. We would not develop language nor could we benefit from experience. In short, we would never develop into the children, adolescents, and adults that we are familiar with.
Rumelhart and McClelland (1986) and McClelland and Rumelhart (1986) provided demonstration proofs that artificial neural networks, called connectionist models, can form memories, can learn, and therefore can do psychology. Connectionist models of many psychological phenomena have been developed. The Psychological Review is a journal that specializes in psychological theory. It has published numerous long articles featuring connectionist neural network models. Many other demonstration proofs have been published in a wide variety of journals and books. Connectionist neural network models now rival traditional cognitive psychology models.
How Psychology Changes Biology
Here I sketch a general explanation that derives from parallel-distributed-processing (PDP) connectionist-neural-network (CNN) models that I collectively refer to as Computational Neuropsychology (CNP). Two major features characterize these models. The first major feature of these models is that they simulate neural architecture by using layers of simulated neurons. The second major feature of these models is that these simulated neurons are connected by simulated synapses. Artificial neural networks learn through training that modifies these synapses. Some synapses become more excitatory while others become more inhibitory of received activations. The difference between what the neural network computes as simulated behavior and the desired response is considered to be an error. These errors are used to modify the simulated synapses. These changes simulate the way that experience-dependent plasticity mechanisms modify real synapses in biological neural networks while they learn by forming memories. And then another learning trial begins. The network’s performance gradually improves through additional synaptic modification. Here we can see that learning is mostly about modifying synaptic connections.
But more brain changes are involved in psychological development. Infants are born with far more synapses than they will need as adults. Neural network pathways that are active while learning language, music, reading, writing, and playing sports, among other skills, are biologically reinforced by modifying synapses. Unused synapses are cannibalized to save precious metabolic energy. Psychological development literally, physically, sculpts the brain in addition to modifying synapses and thereby changes biology! Our brains physically specialize as we develop psychologically. This explains why it is more difficult for older people to learn a new language.
How Biology Changes Psychology
Our neural network understanding of how psychology changes biology prepares us to understand how biology modifies psychology. Understanding that the synapses that connect neurons contain our memories of who we are, the people that we know, the experiences we have had, and our attitudes about everyone and everything along with how we feel enables us to see that directly modifying them with legal or illegal psychoactive substances will change our psychology. Psychology normally changes our synapses by activating internal experience-dependent plasticity mechanisms. Drugs directly modify these same synapses pharmacologically and consequently alters our psychology. Pharmacological psychiatry is a relatively young field. The clinical practice of selecting the right medication to make therapeutic synaptic modifications is, by and large, a trial and error business. It can take several weeks for therapeutic effects to be noticed. Therapeutic effects are often dose dependent which means that dosage may need to be systematically increased.
Neural network models enable us to see how psychology changes biology because the memory formation process that drives learning and all psychological development modifies synapses through experience-dependent plasticity neuroscience mechanisms. This knowledge enables to understand that modifying synapses pharmacologically will also change our psychology. The causal role of synapses in learning and memory make them the missing link in psychobiology and biopsychology. I predict that psychology will organize around the synapse when it becomes a mature natural science just as biology organized around the cell when it became a mature natural science. Subsequent blogs will present more by way of fascinating new developments – stay tuned.
- Clinical Implications of Priming in Psychotherapy
- Clinical Implications of Reactivation in Psychotherapy
- Clinical Implications of the Transformation Principle
- Clinical Implications of Learning and Memory
- Clinical Implications of Unconscious Processing
Warren’s book, Cognitive Neuroscience and Psychotherapy: Network Principles for a Unified Theory is available for purchase on the Elsevier Store. Use discount code “STC215” at checkout and save up to 30% on your very own copy.
About the Author
Warren W. Tryon received his undergraduate degree from Ohio Northern University in 1966. He was enrolled in the APA approved Doctoral Program in Clinical Psychology at Kent State University from 1966 – 1970. Upon graduation from Kent State, Dr. Tryon joined the Psychology Department faculty at Fordham University in 1970 as an Assistant Professor. He was promoted to Associate Professor in 1977 and to Full Professor in 1983. Licensed as a psychologist in New York State in 1973, he joined the National Register of Health Service Providers in Psychology in 1976, became a Diplomate in Clinical Psychology from the American Board of Professional Psychology (ABPP) in 1984, was promoted to Fellow of Division 12 (Clinical) of the American Psychological Association in 1994 and a fellow of the American Association of Applied and Preventive Psychology in 1996. Also in 1996 he became a Founder of the Assembly of Behavior Analysis and Therapy.
In 2003 he joined The Academy of Clinical Psychology. He was Director of Clinical Psychology Training from 1997 to 2003, and presently is in the third and final year of phased retirement. He will become Emeritus Professor of Psychology in May 2015 after 45 years of service to Fordham University. Dr. Tryon has published 179 titles, including 3 books, 22 chapters, and 140 articles in peer reviewed journals covering statistics, neuropsychology, and clinical psychology. He has reviewed manuscripts for 45 journals and book publishers and has authored 145 papers/posters that were presented at major scientific meetings. Dr. Tryon has mentored 87 doctoral dissertations to completion. This is a record number of completed dissertations at the Fordham University Graduate School of Arts and Sciences and likely elsewhere.
His academic lineage is as follows. His mentor was V. Edwin Bixenstein who studied with O. Hobart Mowrer at the University of Illinois who studied with Knight Dunlap at Johns Hopkins University who studied with Hugo Munsterberg at Harvard University who studied with Wilhelm Wundt at the University of Leipzig.
Cognitive Neuroscience and Psychotherapy: Network Principles for a Unified Theory is Dr. Tryon’s capstone publication. It is the product of more than a quarter of a century of scholarship. Additional material added after this book was printed is available at www.fordham.edu/psychology/tryon. This includes chapter supplements, a color version of Figure 5.6, and a thirteenth “Final Evaluation” chapter. He is on LinkedIn and Facebook. His email address is firstname.lastname@example.org.
This blog and all others by Dr. Warren Tryon can be found on his Fordham faculty webpage.
- Carlson, N. R., Miller, H., Heth, C. D., Donahoe, J. W., & Martin, G. N. (2010). Psychology: The science of behavior (7th ed.) (p. 196); Boston: Allyn & Bacon.
- Kirsch, I., Deacon, B. J., Huedo-Medina, T. B. H., Scoboria, A., Moore, T. J., & Johnson, B. T. (2008). Initial severity and antidepressant benefits: A meta-analysis of data submitted to the Food and Drug Administration. PLoS Medicine, 5, 260-268.
- Kirsch, I., & Sapirstein, G. (1998) Listening to Prozac but hearing placebo: a meta-analysis of antidepressant medication. Prevention and treatment, Vol. I, article 0002a, posted June 26, 1998, available at http://journals.apa.org/prevention/volume1/pre0010002a.html.
- McClelland, J. L., Rumelhart, D. E., & the PDP Research Group (1986). Parallel distributed processing: Explorations in the microstructure of cognition, Vol. 2: Psychological and biological models. Cambridge, MA: MIT Press.
- Rumelhart, D. E., McClelland, J. L., & the PDP Research Group (1986). Parallel distributed processing: Explorations in the microstructure of cognition, Vol. 1: Foundations. Cambridge, MA: MIT Press.
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